Diet-Heart Denialism

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Diet-Heart Denialism

Postby RichardK » Mon Apr 15, 2013 10:56 am

The meta-analysis by Siri-Tarino et al (2010) initiated the birth of neo-diet-heart denialism online. The new gospel is that saturated fats do not contribute to heart disease. Inspired by HealthyLongevity (well, I copied his material), I decided to wrap a forum post pointing out some of the key concepts of diet-heart research. Having rudimental knowledge over these themes helps the inquiring reader to avoid being confused by the professional denialists working hard to confuse their global audience (Gary Taubes, Denise Minger, Stephan Guyenet, etc).

1) Interindividual varition; individual differences in the response to the dose

The differences in fat intake are usually minor in homogeneous cultures. However, the cholesterol levels in every population follows a normal distribution: a same diet will lead to wide variety of cholesterol levels between individuals, even though everything else is kept constant. If the differences in the fat intake are small in a given population, it cannot explain the large differences in serum cholesterol levels in a model. Jacobs et al (1) showed mathematically that null association is expected between diet and serum cholesterol levels in cross-sectional population studies (even when there exist cause and effect): despite the null associations in such studies, the intake of saturated fats is one of primary determinants of serum cholesterol levels of an individual (Pedersen et al 2011).

2) Intraindividual variation (regression dilution bias); spontaneous variation within individual

”Similar lack of attention to intraindividual variability is frequent in surveys and epidemiological studies and leads to error, controversy, and waste of time and money.” (Keys, 1988)

For a long time, Keys held an intellectual monopoly over this theme. In the past, the researchers didn't properly understood that there's a substantial, spontaneous day-to-day (5 to 10%) variation of cholesterol levels within individual, even though the diet is held constant. Hegstedt & Nicolosi (1987) showed that it takes at least 3 blood cholesterol measurement at the baseline of the survey in order to reliable assess the serum cholesterol level of an individual. In addition, twenty-two randomly collected 24-h dietary recalls are required to estimate the true individual mean intake of saturated fat within ±20 %, while most studies have only one recall or a food frequency measure of saturated fat intake available (2). In older studies, participants were often misclassified in wrong categories in regards to both SFA intake and serum cholesterol levels because of inadequate emphasis on intraindividual variation. In other words, an inadequate number of cholesterol measurements and dietary recalls were performed for the participants at the baseline of the survey. This resulted often in null associations of both diet and serum cholesterol levels and eventually between diet and the risk of CHD.

The Seven Countries Study

When Keys (1988) decided to analyze the participants of the large Israel Ischemic Heart Disease study in the form of small groups based on place of birth, he found a strong correlation between the intake of saturated fat and serum cholesterol levels (3). This association did not exist when the participants were analyzed as an individual basis. Some information is always lost with the use of medians, however, by using and comparing medians, the researchers can effectively eliminate the effect of spontaneous variation within individuals (part 2) and the large individual differences in dose-response and the statistical fallacy brought by such large differences between individuals (part 1). Keys understood these two key concepts of diet-heart research already in the late 1950's. He was several decades ahead the curve. The differences in the intake of saturated fat explained 89% of the variation in serum cholesterol levels between the 16 different cohorts used in the 7CS. The differences in the intake of SFAs were large, from 3 percent (of calories) to 22 percent (of calories). The lowest mean serum cholesterol levels at the baseline was measured in one of the Japanese cohort (143mg/dl) and the highest in one of the Finnish cohort (262mg/dl). These ecologic correlations described the real world in much greater accuracy than did the poorly conducted population studies from homogeneous cultures. The ecologic correlations between diet and serum cholesterol levels were similar to the results obtained from tightly controlled metabolic-ward feeding trials. Neo-diet-heart denialists such as Guyenet and Taubes attempt to confuse the reader by showing a cascade of old cross-sectional and prospective cohorts in order to demonstrate that the intake of SFAs do not affect the risk of CHD: The poor audience is left out with an impression that the science is a democracy where every study bears an equal value*

*Bonus

It has been pointed out (4) that regression dilution bias dilutes the real association of serum cholesterol concentration and the risk of CHD in several large-scale prospective population studies such as the Framingham and Whitehall. Moreover, the infamous meta-analysis by Siri-Tarino et al used poorly conducted sub-studies that did not pay attention to regression dilution bias and/or were adjusted for serum cholesterol levels (see Stamler 2010; Katan et al 2011; Scarborough et al 2010; Kromhout et al 2011 and Pedersen et al 2011). Modern forward-looking studies, with sophisticated dietary recall techniques, paying careful attention to intraindividual variation, such as the Health Professional’s Follow-up (5) found that saturated fat intake was associated with a statistically significant 72% increased risk of fatal coronary heart disease for high compared to low intake (after maximum adjustment).

Links to some of the references used:

1) http://aje.oxfordjournals.org/content/110/1/77.short

2) http://arc.crsociety.org/read.php?3,206528

3) http://ajcn.nutrition.org/content/48/5/1161.short

4) http://aje.oxfordjournals.org/content/1 ... 1.full.pdf

5) http://www.ncbi.nlm.nih.gov/pubmed/8688759
Last edited by RichardK on Tue Apr 16, 2013 8:11 am, edited 2 times in total.
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Re: Diet-Heart Denialism.

Postby Spiral » Tue Apr 16, 2013 3:17 am

This is an excellent post with lots of great information. Thank you.
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Re: Diet-Heart Denialism.

Postby RichardK » Tue Apr 16, 2013 5:43 am

^Thank you!

PlantPositive covered these themes as well in his video "measurement problem".

http://www.youtube.com/watch?feature=pl ... ZK2J5ln5jg
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Re: Diet-Heart Denialism.

Postby veggylvr » Tue Apr 16, 2013 5:58 am

Great post, though hard to understand. Wish you (or someone) could summarize it in easier language for us to convey.
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Re: Diet-Heart Denialism.

Postby RichardK » Tue Apr 16, 2013 6:45 am

^Don't stress. This was more sort of a aficionado post for the geeks :)
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Re: Diet-Heart Denialism.

Postby veggylvr » Tue Apr 16, 2013 6:54 am

RichardK wrote:^Don't stress. This was more sort of a aficionado post for the geeks :)


Yes, I realize, and I'm going to save it. But in a verbal argument with one of these denialists, I'm not sure how I could respond.
A brief, easier summary would be helpful.
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Re: Diet-Heart Denialism

Postby healthy-longevity » Tue Apr 16, 2013 8:33 am

As addressed in my diet-heart posts, there is convincing evidence from hundreds of rigorously controlled feeding experiments that dietary cholesterol (when baseline intake is low) and isocaloric substitution of saturated fat (lauric, myristic and palmitic acids) for carbohydrate, polyunsaturated fat and monounsaturated fat raises LDL cholesterol. In addition there is convincing evidence from over 100 lipid modifying interventions and mendelian randomization studies with over 300,000 individuals that lowering LDL cholesterol significantly lowers the risk of coronary heart disease, independent of particle size, HDL cholesterol, triglycerides and non-lipid effects of specific interventions.

Furthermore, it has been demonstrated in thousands of experiments that the feeding of cholesterol and saturated fat will accelerate the formation of atherosclerosis in virtually every vertebrate that has been sufficiently challenged. This includes mammalian, avian and fish species- herbivores, omnivores and carnivores, and over one dozen different species of nonhuman primates.

These are perhaps some of the strongest forms of evidence supporting the diet-heart hypothesis, although there are other forms of supportive evidence. The skeptics of the diet-heart hypothesis ignore this evidence and have attempted to distract their audience with other forms of evidence that are problematic and insufficient to refute the hypothesis. Richard provides several explanations as to why these forms of evidence that the skeptics select are problematic.

One major concern of the within-population studies that Richard describes is intraindividual (within-person) variation. If the within-person variation is larger than the between-person variation, which is common in homogenous populations where everyone consumes a similar diet, then this will especially bias the findings towards a null association. For example, in a homogenous population with a between-person variation of between 2 to 6 eggs per week on average, the variation of intake of an individual consuming on average 4 eggs per week maybe between 1 to 7 eggs per week. If this person’s diet is measured at a high or low point they will be misclassified into a high or low range of intake, typically biasing the results towards a null association.

Another concern is related to the fact that observational studies addressing the association between diet and blood cholesterol and cardiovascular disease dating back to at least the early 1950s have been complicated by reverse causation. It is well documented that people will lower intake of cholesterol and saturated fat in response to elevated blood cholesterol. This is known to bias studies towards finding an association between a higher intake of cholesterol and saturated fat and lower blood cholesterol levels. This would also likely similarly bias the results for the association between intake of cholesterol and saturated fat and the risk of cardiovascular disease.

One other major concern is that most studies do not compare saturated fat to appropriate substitutes such as complex carbohydrates, and is instead compared to all other sources of calories combined, which is predominantly junk food.
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Re: Diet-Heart Denialism

Postby RichardK » Tue Apr 16, 2013 8:51 am

^HealthyL,

thanks for the additional comments.

"Parallel to the lack of association between saturated fat intake and CHD risk, as shown in the meta-analysis, is the lack of association between dietary saturated fat and serum cholesterol in cross-sectional analyses of the Framingham, Tecumseh and Zutphen studies(6-8). Keys(9) explained the lack of an association between dietary saturated fat and serum cholesterol in cross-sectional studies by the large day-to-day variation within individuals in both saturated fat intake and serum cholesterol. He showed that the intra-individual variance of the SFA palmitic acid was more than twice as large as the inter-individual variance, based on two measurements. He also found that in healthy adults on an ostensibly constant diet, the average intra-individual standard deviation of serum cholesterol was approximately 200 mg/l (20 mg/dl), about half the total standard deviation(9)”.

Kromhout et al 2011

Veggy wanted some kind of a down-to-earth explanation. I am afraid I am not able to deliver such explanation. But let me share you one example in regards to interindividual variation.

Let's imagine we have 100 people who all eat the McDougall-diet. The mean serum cholesterol level of this group is 130mg/dl. However, some people in this group have their total cholesterol level at 89mg/dl and some at 160mg/dl. The primary reason why everyone have these low levels is because the intake of saturated fats (and dietary cholesterol) is so low in the diets of these 100 people. However, since there are virtually no variation in the intake of saturated fat in this group, the utilized statistical model cannot show that the intake of saturated fat (and/or dietary cholesterol) explains the differences in the cholesterol levels observed in the members of the group. This is just one theme that the diet-heart research must address.

As Pedersen et al (2011) concluded in regards to Siri-Tarino et al:

“That replacement of SFA by a variety of carbohydrate-containing foods also reduces CHD risk may be inferred from ecological studies, e.g. in Finland. CHD was also almost non-existent in rural China when mean cholesterol levels were approximately 3·5 mmol/l (1350 mg/l), with total fat intakes only about 15% of energy and extremely low intakes of SFA(10,11). These observations, replicated in many other countries, should not be ignored even if meta-analyses of prospective cohort studies suggest no independent associations of SFA intake with CHD risk(2). The null results of the latter studies(2) probably reflect measurement error, residual confounding, over-adjustment by covariates on the causal pathway and large variations in plasma cholesterol compared to variations in intake of dietary fat(3,12 – 15). The role of SFA risks may also be overlooked, given the strong emphasis on TFA(16) and the incorrect proposition that the CHD epidemic in affluent societies has been primarily linked to a high consumption of TFA(17)”
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